Case Study
A rapid response event was initiated by the bedside nurse for a patient with a heart rate of 44 beats per min (bpm) on the telemonitor. On prompt arrival of the rapid response team, it was noted that the patient was a 64-year-old male with comorbidities of chronic systolic heart failure, atrial fibrillation, and osteoarthritis, who was admitted three days ago for severe gastroenteritis and dehydration. The patient was receiving IV fluids since admission but was unable to get any fluids this day since he refused to be hooked up to continuous infusion. He had also refused any blood draws this morning. The patient was receiving metoprolol, apixaban, aspirin, lisinopril, and digoxin. Pacer pads were attached to the patient in preparation for any need for cardiac pacing.
Vital Signs
Temperature: 98.6 °F
Blood Pressure: 90/60 mmHg
Heart Rate: 45 beats per min – with junctional bradycardia and narrow QRS complexes on telemonitor ( Fig. 11.1 )
Fig. 11.1
Telemetry strip showing junctional bradycardia with inverted P and T waves with a narrow QRS complex.
Respiratory Rate: 14 breaths per min
Pulse Oximetry: 94% oxygen saturation on room air
Focused Physical Examination
The patient was a middle-aged man sitting up in bed, leaning forward in obvious distress. The room was filled with an unmistakable smell of fecal matter. Before examining the patient, it was ensured that everyone had proper protective gowns, surgical gloves, and surgical masks on. The patient’s heart auscultation revealed bradycardia, no prominent murmurs. Chest auscultation was clear. His abdominal exam showed diffuse tenderness. When asked, the patient reported that this started a few hours ago, and he did not report this to the nurse as he thought this might be from his continued diarrhea. He denied pain anywhere else in the body.
Interventions
A stat electrocardiogram (EKG) was ordered, along with a troponin level and electrolytes. The patient was given 1000 cc Plasma-Lyte bolus. EKG obtained showed sinus bradycardia, with occasional breaks of junctional rhythm, depressed T waves, and ST depression in the lateral leads. His last laboratory tests showed that he was hypokalemic with a potassium of 2.8. Patient’s potassium was being corrected intravenously till one day ago; however, he had refused medications and fluids today. With this history in mind, it was decided that this patient might be suffering from hypokalemia induced digitalis toxicity. He was given one dose of atropine (0.5 mg IV) and started on intravenous potassium supplementation. His heart rate and blood pressure improved to 55 bpm and 100/60 mmHg, respectively. Further labs were sent, including a lactate level, digoxin level, and magnesium level. It was decided to transfer him to the cardiac care unit for closer monitoring and possible need of digoxin-specific Fab fragments.
Final Diagnosis:Hypokalemia Induced Digoxin Toxicity Resulting in Sinus Dysfunction
Digoxin Toxicity
Digoxin is one of the oldest drugs for the treatment of heart failure. It was first described for heart failure treatment in 1785 as a component of the plant digitalis purpura. Although it has been in and out of favor by different cardiology guidelines, we have been seeing more and more physicians prescribing digoxin as a treatment for heart failure because of its inotropic effects on cardiac myocytes and rate-controlling agent in atrial fibrillation. The drug works by reversibly inhibiting Na-K-ATPase, leading to increased intracellular sodium and decreased intracellular potassium. Since digoxin binds to the potassium site of Na-K-ATPase, low potassium levels can lead to increased effects of digoxin, leading to toxicity. This mechanism and its interactions with multiple electrolytes have led to the establishment of a very narrow therapeutic index. When the patient is receiving digoxin, the optimal levels of potassium are supposed to be between 4 meq/dL and 5 meq/dL. Explanation of the complete pharmacokinetics for the development of toxicity from digoxin is out of the scope of this chapter, but we will explain what to look for in a patient on digoxin who has cardiac rhythm abnormalities or other signs of toxicity.
Definition and Diagnosis
Digoxin toxicity, also known as digoxin poisoning, is when digoxin acts at an excess to its desired level of activity. This definition is broad, but it tells us that a person does not need to ingest more digoxin to get toxic levels in the system, such as in our case, the therapeutic dose of digoxin was continued, but because of hypokalemia, there was a disproportionate effect of digoxin on the heart.
Digoxin toxicity is a clinical diagnosis based on a history of exposure, suggestive clinical features, and electrocardiac manifestations ( Table 11.1 ). Serum digoxin levels do not always correlate with toxicity, and toxicity can develop with normal serum levels of digoxin. See Table 11.2 for a list of common differential diagnoses of digoxin toxicity.
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